The present invention generally relates to methods and devices for medical or surgical therapy. More particularly, the invention relates to methods and devices for augmenting a sphincter, such as the lower esophageal sphincter, or body lumens, such as the female urethra.
A variety of human ailments arise from the weakening of tissues surrounding body lumens and cavities due to disease, trauma, advancing age, or combinations of these causes. Of particular interest to the present invention, a condition known as gastroesophageal reflux disease or “GERD,” arises when the lower esophageal sphincter (“LES”) weakens and permits the contents of the stomach to move back into the esophagus. Similarly, fecal incontinence can occur when the anal sphincter becomes weakened and ceases to function properly. Female urinary incontinence can occur with weakening of the urethra which is responsible for containing the contents of the bladder. Male urinary incontinence arises with damage to the urinary sphincter. The outlet of the stomach is controlled by the pyloric sphincter. Decreased muscle tone in the pyloric sphincter can lead to rapid gastric emptying which can cause digestive distress.
The human gastrointestinal tract begins at the mouth, and includes the pharynx, esophagus, stomach, small and large intestines, and rectum. Small, ring-like muscles, called sphincters, surround portions of the gastrointestinal tract. In a healthy person, these muscles contract in a coordinated fashion during eating and digestion to temporarily separate one region of the alimentary canal from an other. One example of a gastrointestinal sphincter is the anal sphincter, which provides fecal continence. Another example is the muscular ring called the lower esophageal sphincter (“LES”), which surrounds the opening between the esophagus and the stomach.
Normally, the LES relaxes to allow food to pass from the esophagus to the stomach and contracts to prevent food in the stomach from refluxing backwards into the esophagus. Stomach muscles churn food and digestive juices into a mass called chyme. The muscles then squeeze the chyme toward the opposite, intestinal end of the stomach by peristaltic waves, which start at the top of the stomach and move downward. The pyloric sphincter, another ring-like muscle, eventually relaxes to allow stomach contents to enter the first part of the small intestine. If the LES does not contract properly, however, chyme and other stomach contents may be pushed back into the esophagus causing the painful symptom of heartburn and, potentially permanent damage to the esophageal wall. This insufficiency of the LES, accompanied by regurgitation of stomach contents into the esophagus, is commonly referred to as gastroesophageal reflux disease, or “GERD.”
Gastrointestinal reflux disease is a common disorder, with an estimated two percent of the adult population suffering from the syndrome. The incidence of GERD increases markedly after the age of 40, and it is not uncommon for patients experiencing symptoms to wait years before seeking medical treatment. Postponing treatment can lead to further health concerns, as continued presence of acid in the esophagus may lead to permanent damage of the esophagus. It has also been hypothesized that such esophageal damage may be a precursor to esophageal cancer.
Generally, many factors are thought to potentially contribute to the occurrence of GERD. For example, transient LES relaxation, decreased LES resting tone, impaired esophageal clearance, delayed gastric emptying, decreased salivation, and impaired tissue resistance all may contribute to causing GERD. Lifestyle factors may also contribute to cause reflux. Smoking, large meals, fatty foods, caffeine, pregnancy, obesity, body position, drugs, hormones, and paraplegia may all exacerbate GERD. Also, hiatal hernias frequently accompany severe cases of GIERD.
In addition to heartburn, other frequently reported symptoms of GERD include painful swallowing, difficulty swallowing, pulmonary symptoms such as coughing, wheezing, asthma, aspiration pneumonia, and interstitial fibrosis, oral symptoms such as tooth enamel decay, gingivitis, and halitosis, throat symptoms such as a soreness, laryngitis, hoarseness, and a globus sensation; and earache. As mentioned briefly above, complications of GERD include esophageal damages, such as erosion, esophageal ulcer, and esophageal stricture; replacement of normal esophageal epithelium with abnormal (Barrett's) epithelium; and pulmonary aspiration. Barrett's epithelium, in turn, may be a precursor to esophageal cancer.
Currently available therapies for treatment of GERD generally focus on pharmaceutical therapy and surgery. Drug therapies typically reduce or block stomach acid secretions, but do not strengthen or otherwise treat the LES. Surgical intervention typically includes procedures which attempt to create a sphincter-like mechanism at the site of the LES. Nissen fundoplication, for example, is an abdominal surgery that involves freeing a portion of the stomach from surrounding connective tissue, wrapping it around the outside of the esophagus at approximately the location of the LES, and attaching it back to another part of the stomach. Although this procedure often successfully tightens the esophagus at an area near the LES and may succeed in preventing GERD, it is often difficult to gauge how tight or loose to wrap the stomach—if wrapped too tightly, food has difficulty passing into the stomach, if wrapped too loosely, GERD will not be prevented.
Thus, GERD is a very prevalent condition with numerous painful symptoms, potentially serious complications, and relatively few viable treatment options. Therefore, it would be advantageous to have methods and devices to augment the LES to prevent or treat GERD. Ideally, such methods and devices would provide for long-lasting or even permanent treatment of the LES in a non-invasive or minimally invasive manner. Additionally, it would be beneficial if such methods and devices could be used in treating other body sphincters, such as the anal sphincter to treat fecal incontinence.
Urinary incontinence arises in both men and women with varying degrees of severity and from different causes. In men, the condition frequently occurs as a result of prostatectomies which damage the urinary sphincter. In women, the condition typically arises after pregnancy where stretching of the structure supporting the urinary tract can weaken the urethra.
A number of approaches have been developed for treating urinary incontinence. Of particular interest to the present invention, techniques have been developed for injecting collagen or other bulking agents into tissues surrounding the urethra in women and the urinary sphincter in men. While these treatments are at least partly successful, it would be beneficial to provide alternative treatments. Bulking agents, such as collagen, are resorbed and thus provide only temporary relief. Most persistent and substantial bulking agents can evert the sphincter and prevent its normal functioning.
Thus, it would be desirable to provide methods and systems for bulking or toning the sphincter. In particular, it would be desirable to be able to augment the sphincter sufficiently to keep the sphincter closed until sufficient force is applied to open the sphincter, at which point the closing force would drop off significantly. Similarly, with urinary incontinence, present bulking agents will cause closing of the urinary tract before the bladder has completely emptied. An approach which allowed the urinary tract to remain open longer would be beneficial. The present invention can at least partly meet these goals by providing a bulking or closing force which, once a lumen is opened, drops off rapidly to allow the lumen to remain open until opening forces fall to a very low point.